The present invention relates to revitalizing layers of the skin which have been damaged by the environment. More specifically sunlight exposure and particularly ultraviolet radiation can cause a variety of skin changes and damages such as premature aging, and skin cancer. There are three main types of UV radiation, UVA, UVB, and UVC. UVC has the shortest wavelength. UVA on the other hand has the longest wavelength. However, as with any electromagnetic energy, the shortest wavelength is the most susceptible to obstruction while the longest wavelength is the least. UVC for example is almost completely blocked by the ozone layer in our atmosphere, while UVB penetrates the atmosphere relatively unobstructed and causes damage in the outer layer of the skin. UVB, however, does not penetrate glass. UVA, on the other hand, can penetrate glass and deeper into the skin to cause skin damage.
On a cellular level, UV radiation can cause collagen breakdown, creation of free radicals, interfere with DNA repair, and suppress the immune system's ability to survey and destroy cancerous cells. Of these damaging effects, perhaps the most significant is the creation of free radicals.
Oxygen molecules normally exist in stably bonded pairs. Free radicals are created when ionizing energy like UV radiation strikes a stable, paired oxygen molecule splitting its paired electron bonding, resulting in two single oxygen molecules. These two oxygen molecules each have one unpaired valence electron that is very reactive inside human tissues and cells. These free radical oxygen molecules react with organic molecules in the connective tissue and cells stealing electrons away from structures that require those electrons for stable bonds. This causes damage to enzymes, DNA's, collagen structures and cell wall stability and permeability. Damage to these cellular structures can cause for example: DNA mutations (that lead to cancerous behavior); suppression of enzymatic functions that regulate cellular signaling, apoptosis, immune functions, as well as, DNA repair.
One well known skin condition that occurs as a result of prolonged, cumulative effect of sun exposure is Actinic Keratosis, (AK's). AK's are by far the most common skin lesion with malignant potential on the skin. These lesions develop in a stepwise progression from subclinical skin changes to overt, invasive Squamous Cell Carcinoma, (SCC). If left untreated, these AK lesions have 1 per 1000 per year chance of becoming cancerous.
Clinically, AK's present with a range of characteristics. They can be barely perceptible to rough, elevated hyperkeratotic plagues several centimeters in diameter. The base may be light or dark, tan, pink, red, or a combination of these. Most typically though, they appear as multiple discrete lesions that are small crusty, scaly or crumbly bump or horn on an erythematous base.
Histologically, AK's share features with SCC. The histological characteristics are as follows: AK's are located in the epidermis and show hyperkeratosis with intermittent large parakeratotic nuclei and occasional mitotic figures; keratinocyte atypia along the basal layer; spongiosis in the immediate suprabasalar layer; budding of the basal layer keratinocytes into the dermis; perivascular inflammation and solar elastosis.
Treatment of AK's typically consists of surgical destruction. The difficulty with surgical destruction is that it is difficult and impractical to treat a large area of the skin that has large number of lesions.